Problem-Fractures-Brian-Simpson (correct copy)

INTRODUCTION
Most Chartered Physiotherapists deal with musculo-skeletal injuries.......or do
they?
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There is no doubt that MSk physios deal with structures that attach to the skeleton
muscles, ligaments, tendons, joint capsules etc., but very few actually ever treat
the skeleton per se when it becomes injured.
We will be discussing what types of modalities can be used to treat the problem
skeletal injuries i.e. delayed or non-union fractures. We will discuss the different
types of non-union, why they continue to be non-union and how physiotherapists
can influence the healing rate of such non-unions by the use of certain treatment
modalities which have extensive evidence to support their efficacy.
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PHYSIOLOGY AND STRUCTURE
Before being able to treat bone, clinicians should re-acquaint themselves with the
physiology of bone and the manner by which physiotherapists can influence that
physiology to the benefit of the patient and the satisfaction of the orthopaedic
surgeon.
Bone is the only body structure requiring longitudinal compressive strength as well
as the ability to be able to withstand lateral and rotational forces. If bone were
constructed as a solid block it would be able to absorb longitudinal compression
but would easily snap whenever lateral or rotational forces were applied e.g.
coral or a stick of Blackpool rock. Osteopetrosis and pycnodysostosis are both
congenital conditions involving very dense, abnormal bones which fracture very
readily and heal badly e.g. Toulouse-Lautrec. However, bone consists mainly of
hydroxyapatite a bi-crystalline form of calcium phosphate and collagen fibres.
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Bone responds to compression forces by generating a piezo-electric flow of current
along the length of the bone. This current flow stimulates osteoblasts to deposit
more bone along the track of the current, enabling bones to thicken in response to
increased load e.g. weight gain, change in sporting activity levels etc.
Bone at the nanoscale
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When stress/pressure is applied to bone, this is absorbed by soft layers at successively lower length
scales and less than 20% is noticed in the mineral phase. This strain induces a piezo-electric current
which is vital for re-modelling and bone maintenance. NWB reduces this potential osteopaenia.
The soft structures (collagen) form a single rigid unit at the next level and so on, enabling the tissues to
sustain large strains. Hence, brittle apatite remains shielded from excessive loads and does not break.
Mineral crystallites are, nonetheless, very strong, capable of carrying more than 2-3 times the fracture
load of bulk apatite.
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(Max Planck Inst. And European Synchrotron Radiation Facility
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Compare with glass fibre mat, epoxy resin and GRP.
Yellow cylinders = mineralised collagen
fibrils in longitudinal section
Red tablets = mineral apatite crystallites
embedded within the collagenous matrix of
the fibrils
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Bone exists as :1) Cortical bone which has high density, low surface area and low remodelling rates. It is mostly present in the femoral neck and shafts of long
bones.
2) Trabecular bone which has low density, high surface area and high remodelling rates and is mostly present in vertebral bodies and calcaneum.
3) Periosteum is very important for normal vascularity and is an important
source of bone-forming cells. Periosteum is very well innervated.
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4) Osteoblasts are cuboidal and mono-nucleated with basophilic cytoplasm.
Their role is to form new bone. NB they exhibit a strong histochemical
reaction for Alkaline Phosphatase (ALP). When mature, they synthesise
Type 1 collagen but in non-unions they express Type III collagen. 2 They
are attracted to, and migrate to, areas of bone with a ve net potential.
5) Osteoclasts are multi-nucleated and are responsible for bone resorption.
They test strongly for Tartrate Resisitant Acid Phosphatase (TRAP) and are
attracted to, and migrate to, areas of bone with net +ve electrical potential.
Osteoclast apoptosis is delayed by oestrogen deficiency.
6) Stromal cells produce growth factors for haemopoiesis and help the
formation of osteoclasts as well as having the ability to differentiate to
osteoblasts,
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Bone allows the flow of blood and lymph through the medulla and Haversian
vessels and also via the periosteum. Disruption of this blood supply and failure to
re-establish a normal circulatory flow through the fracture is the principal reason
for delayed and non-union.
Blood supply to bone.
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The skeleton receives 10-20% of the cardiac output.
Blood vessels especially rich in areas containing red bone marrow.
Bone drains via veins that accompany the arteries and through foramina
near the articular ends of bones i.e. haemopoietic region.
Lymph vessels are abundant in the periosteum BUT new research
suggests lymph vessels are much more extensive and vital for
drainage. (Prof. Tony Pohl) 3
Because bone has no ability to accommodate swelling, impairment of
drainage can result in the ultimate compartment syndrome.
Vascular stasis results in local hypoxia or even anoxia with tissue necrosis
(similar to varicose ulcers)
Reduced drainage causes metabolite accumulation
H2CO3, pyruvic acid,
lactic acid etc. which may attract acidophilic cells i.e. osteoclasts and
produce a hostile environment for basophilic osteoblasts.
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Blood supply to bone
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Epiphyseal arteries
Metaphyseal arteries
Diaphyseal nutrient artery
Arterial anastamoses
NB Seldom mention in text books of
bone vascular drainage.
Reasons for Non-Union
It is well known that fractures in poorly vascularised bones such as scaphoid, neck
of talus and the junction of the middle and lower thirds of the tibia have a much
greater tendency to progress to non-union. High speed trauma may involve
extensive displacement at the fracture site with resultant periosteal stripping and
further vascular damage. Pollution of bone ends in compound fractures may
introduce pathogens which can further interfere with blood supply.
Types of Non-Union
Hypertrophic- extensive callus formation with good vascularity but no complete
bridging. This type of non-union probably is due to inadequate immobilisation.
These respond well to proper stabilisation and good therapeutic management.
Atrophic- absence of callus and atrophic bone ends which may appear tapered and
osteopaenic, but are sometimes sclerotic. Bone vascularity is very poor with poor
healing potential. There are two sub-types·
Simple atrophic- has the potential to respond to
treatment to encourage angio-neo-genesis
Synovial atrophic- forms a fibrous fluid filled capsule
around the bone ends and is referred to as a synovial pseudarthrosis. Bones
such as the clavicle can comfortably tolerate a synovial pseudarthrosis with
little pain or reduction in function. Non-surgical treatment of synovial
pseudarthrosis will almost certainly not achieve bony union. Removal of the
capsule and freshening of the bone ends is essential.
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Normatrophic- both ends have moderate vascularity and have moderate healing
potential. This type of non-union is eminently suitable for treatment by several
modalities.
TREATMENT MODALITIES
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Pulsed Magnetic Field Therapy (PMFT) in the treatment of fractures is defined
as the application of time varying magnetic fields that induce voltage wave form
patterns in bone similar to these resulting from mechanical deformation. 4 The
voltage is induced at right angles to the pulsed or dynamic magnetic field.
Magnetic field strength in clinical application ranges from 30G to 1000G (the
-200Hz.
PMFT was approved by the FDA in 1979 for the treatment of fractures and nonunion fractures.
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Pulsed Magnetic Fields
Electro-magnetic induction
PMFT
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Dynamic magnetic field
Induced electrical field
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The application of time-varying Magnetic fields that induce voltage
wave-form patterns in bone similar to those resulting from
weight-bearing and mechanical deformation (Strain potential)
Therapeutic magnetic field strength from 30G to > 1,000G ( Earth s
magnetic field IRO 0.5G) CONVERSION- 10,000G = 1 Tesla
Frequency range 1Hz to 200 Hz typically used
Magnetic fields penetrate virtually everything POP not a barrier
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A literature review by Gossling et al in 1992 13 concluded that PMFT alone was at
least as effective as surgery in cases of non-union with success rate of 80% +.
Mooney in 1990, 5 studying the efficacy of PMFT in lumbar inter-body fusions
showed a success rate of 92% in the PMFT group compared to 65% in the nontreated, placebo group. A similar study by Marks in 2000 6 showed 97.6% fusion
rate with PMFT compared to 52.6% in the placebo group.
Bassett et al in 1982 7 showed in a group of patients with an average of 4.7 years
of non-union, 3.4 previous surgical failures and 35% infection rate, bone healing
took place in 75% of patients.
The effects PMFT observed in bone in fracture non-unions and failed arthrodeses
involved angiogenesis, increased mineralisation, increase in endochondral
ossification, increase in osteoblastic activity and decrease in osteoclastic activity.
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PMFT penetrates anything, including POP and Baycast. Metal implants do not
-thermic.
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LASER
Therapeutic lasers are coherent, mono-chromatic light emissions. Some laser
diodes have up to 6 degree divergent beams, thus obeying the Inverse Square Law
but many more powerful scanning lasers have non-divergent beams.
Infra-red lasers
Usual frequencies 630nM
(visible) 980nM.
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Intensities 5mW hand-held
pen laser (Class IIIB) to 4W
scanning laser (Class IV)
Therapeutic wavelengths range from 600nm to 1000nm. Outputs range from 5mW
to 3000mW with treatment times varying from mere seconds to several minutes.
Dickson et al 8 showed a 300% increase in ALP expression (indicator of osteoblast
activity) in rat femoral fractures. The main effect is photo chemical and not
thermic.
Yaakobi and Oron 9 showed that 630nm irradiation of the rat tibia caused a 120%
increase in ALP and a 40% reduction in TRAP, and that at 13 days reparative
compact bone was measured at 88% against 44% in non-irradiated animals.
Low Intensity Pulsed Ultra-Sound
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LIPUS
LIPUS uses an output of about 1MHz at an intensity of 20mW/cm2 up to
200mW/cm2. LIPUS was approved by the FDA in 1994 for the accelerated healing
of fresh fractures and in 2000 for the healing of established non-union fractures.
The studies presented to the FDA showed that LIPUS had a positive effect by
enhancing angiogenesis, chondrogenesis and osteogenesis.
Low Intensity Pulsed Ultra Sound - LIPUS
Gross et al in 1997 10 suggested that, as LIPUS energy is absorbed at a rate
proportional to tissue density, gradients of mechanical stress would be produced
when applied to a callus where cartilage/bone/collagen interfaces abound. Wallace
et al in 1994 14 showed that there was stimulation of vascular activity as part of a
bone
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World-wide clinical studies using LIPUS for the treatment of non-unions
demonstrated a healing rate of 88% in non-unions presenting with an average of 23
months since fracture. When compared with surgery, LIPUS for non-unions has
the same success rate as surgery.
The study by Heckmann et al 11 in 1994 on delayed union tibial fractures showed
only 6% progressing to full non-union compared to 36% non-unions in the control
group.
HYPERBARIC OXYGEN THERAPY (HBOT)
HBOT involves breathing100% medical oxygen while lying or sitting in a
compression chamber in which the surrounding pressure is at about double normal
atmospheric pressure. Normal air is about 20% O2, so breathing 100% O2 at double
atmospheric pressure can cause up to a 10 fold increase in O2 levels dissolved in
the concentration
the plasma
of a gas in a fluid is determined by pressure and the solubility of the gas . RBCs
supply O2 directly to brain cells and muscle fibres but most cells are oxygenated by
dissolved O2 in the plasma. Lack of O2 is thought to be a limiting factor in fracture
healing. Multipotential precursors of fibroplastic origin form cartilage which is
relatively avascular in the presence of low pO2 but form bone when tissue pO2 is
elevated. 12
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Hyperbaric oxygen therapy
Effects of HBO
2ATA (10 metre depth)+ 100%
O2 .
Peripheral vaso-constriction with
capillary twigging .
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Raising of plasma O2 levels by up
to 10X.
Angioneogenesis with raised O2
in plasma reduce extent of
necrosis.
Mitochondria utilise 80% of the molecular O2 with the other 20% being taken up
by microsomes, nuclei and plasma membranes. In trauma, where local blood
vessels have been destroyed, cells in the centre/ epicentre of the fracture can
become hypoxic or anoxic. Under normal circumstances, the rate of utilisation of
O2 is blood flow limited but, if damaged cells are beyond a critical distance from
the nearest capillaries, then the O2 utilisation becomes diffusion limited. ATP
synthesis can no longer occur and mitochondrial function ceases. Healing cannot
occur until O2 supply is restored, either by angiogenesis or by otherwise increasing
the O2 in the plasma which continues to perfuse the fracture.
It is accepted that most physios would not have access to HBOT.
SUMMARY
A wound is defined as an injury to the body which causes a disruption in the
normal continuity of the body structures. Fractures may be defined as the
disruption of continuity of bone and yet, while physios would expect to
successfully treat wounds in other tissues, they have traditionally drawn a line at
trying to create an ideal healing environment for bone injuries.
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If the aim of treatment is to reduce tissue oedema and thus lower interstitial
pressure, the result is improved vascular flow, increased cellular pO 2 and improved
rate of healing. If the aim of treatment is angiogenesis then there are many options
ve that aim. If the aim of
treatment is to create an optimal physiological environment for healing, then
physiotherapists have been doing just that for years when treating muscles,
ligaments, tendons, skin etc and, with the cooperation of surgeons have the
capability to do precisely the same with bone wounds i.e. fractures.
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References
1) Max Planck Inst. And European Synchrotron Radiation Facility
2) LAWTON DM et al: Mature osteoblasts in human non-union fractures
express Collage Type III. Mol. Path., Vol 50, Issue 4 194-197
3) POHL T. (1999). Bone circulation, the lymphatic system contribution.
4) BASSETT CA: Fundamental and practical aspects of therapeutic uses of
electro-magnetic fields: Crit Rev. Biomech. Eng.; 17(5): 451-529. 1989
5) MOONEY V: A randomised, double-blind prospective study of the efficacy
of pulsed electro-magnetic fields for interbody lumbar fusions. Spine 1990;
15:708-712
6) MARKS RA: Spinal fusion for disco-genic low back pain: outcomes in
patients with or without pulsed electro-magnetic field stimulation. Adv.
Therapy. 2000; 17:57-67
7) BASSET CA, MITCHELLSN, GASTON SR: Pulsing electro-magnetic field
treatment in ununited fractures and failed arthrodeses. JAMA 1982;247
(5):623-628
8) DICKSON et al: The effects of LLLT on alkaline phosphatase expression
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9) YAAKOBI T,ORON U : Effect of Low Level Laser irradiation on the
process of repair in the rat tibia. Dep. Zool., Tel Aviv Uni.
10) GROSS TS et al: Strain gradients correlate with sites of Periosteal bone
formation. J Mone Miner Res. 1997; 12: 982-988
11) HECKMAN JD et al: Acceleration of tibial fracture healing by non-invasive
low intensity pulsed ultra-sound. J Bone + Joint Surg;1994. 76-A,No 1.pp2634
12) BASSETT AC+ HERMANN I: Influence of O2 concentration and
mechanical factors on differentiation of connective tissue in vitro : Nature
190: 460-461. 1961
13) GOSSLING HR, BERNSTEIN RA,ABBOTT J: Treatment of ununited
tibial fractures: a comparison of surgery and pulsed electro-magnetic fields.
Orthopaedics 1992; 15: 711-719
14) WALLACE AL et al: The vascular response to fracture micro-movement.
Cli Orth. 1994;301:281-290